Peripheral blood lymphocytes immunophenotype and serum concentration of soluble HLA class I in burn patients

The level of the soluble form of histocompatibility class I antigens, associated with beta(2)-microglobulin (sHLA-I) has been determined by an ELISA sandwich method in serum from burned patients (n=42) and healthy volunteers (n=30). The sHLA-I level was insignificantly increased in burn patients at the stage of burn shock (1284+/-324U/ml, mean+/-S.E.M.) and after day 28 postburn (1368+/-258U/ml) compared to volunteers (1150+/-90U/ml). At the same time a decrease of sHLA-I levels between 4 and 14 days (638+/-178U/ml) was determined (P<0.05). Increased levels of sHLA, though not significant, were detected in patients with TBSAB >70% in comparison to patients with TBSAB from 30 to 70% during burn shock (1493+/-528 and 1075+/-339U/ml, respectively). Expression of membranous HLA class I antigens (mHLA-I) in peripheral blood lymphocytes (PBLs) was assayed simultaneously by indirect immunofluorescence. The number of CD3(+), CD4(+), CD8(+), CD25(+), CD71(+) and CD26(+) lymphocytes was also evaluated. The expression of mHLA-I in PBLs was increased significantly in patients with TBSAB <70% at early postburn period. Daily monitoring showed that the relative numbers of CD25(+) and CD71(+) lymphocytes in patients varied greatly within short intervals of time during burn shock. The data obtained suggest that mHLA-I expression can reflect postburn lymphocyte activation. The serum content of sHLA-I does not depend on lymphocyte number or activated lymphocyte number in peripheral blood at burned patients.     

风湿性瓣膜病二尖瓣与主动脉瓣置换术1154例长期效果分析

目的　评价风湿性联合瓣膜病二尖瓣与主动脉瓣双瓣置换术的近期与远期疗效 ,分析影响手术疗效的因素。　方法　回顾性分析 1981年 5月～ 2 0 0 1年 5月 2 0年间 ,115 4例风湿性心脏病患者行双瓣膜置换术的临床资料和长期随访结果 ,其中二尖瓣与主动脉瓣均为狭窄病变者 2 5 3例 ,二尖瓣狭窄合并主动脉瓣关闭不全者 345例 ,二尖瓣关闭不全合并主动脉瓣狭窄者 119例 ,二尖瓣与主动脉瓣均为关闭不全者 437例 ;合并三尖瓣病变的占 5 4 0 0 %( 75 7例 ) ,其中器质性病变 7 2 7%( 84例 ) ,功能性关闭不全 5 8 31%( 6 73例 ) ;合并中度以上肺动脉高压者 339例 ;术前NYHA心功能分级Ⅲ级与Ⅳ级者分别为 873例和 186例。应用侧倾碟瓣或双叶机械瓣施行瓣膜置换术 ,合并三尖瓣功能或器质性病变者 ,同期行瓣膜成形手术。　结果　本组患者术后住院病死率为 6 5 0 %( 75 / 115 4)。早期死亡的主要原因为低心排出量综合征、顽固性心律失常、肾功能或呼吸功能衰竭 ,以及抗凝有关的出血等。长期生存 10 79例 ,随访时间为 8个月～ 2 0年 ,平均随访时间为 4 5 %病人·年。晚期死亡 6 6例 ( 0 39%病人·年 ) ;5、10与 15年累计生存率分别为 ( 89 46± 1 35 ) %、( 86 5 0± 1 91) %与 ( 6 7 86±6 16 ) %。生存的 92 9例患     

Tolerogenic role of Kupffer cells in allergic reactions

Drug-induced allergic reactions (DIARs), including allergic hepatitis, cutaneous reactions, and blood dyscrasias, are unpredictable and can be life threatening. Although current studies suggest that DIARs are caused by immunogenic drug-protein adducts, it remains unclear what factors determine the susceptibility to DIARs. We hypothesized that most individuals may be resistant to DIARs in part because they become immunologically tolerant to drug-protein adducts in the liver, an organ with tolerogenic properties. Because animal models of DIARs are elusive, we tested this hypothesis using a murine model of 2,4-dinitrochlorobenzene (DNCB)-induced delayed type hypersensitivity reaction that is mediated by immunogenic 2,4-dinitrophenylated (DNP)-protein adducts. Intravenous pretreatment of mice with DNP-BSA led to its accumulation in hepatic Kupffer cells (KC) and induced immunological tolerance to subsequent DNCB sensitization. Tolerance could be abrogated by prior depletion of KC or induced in na?ve mice by transferring a T cell-depleted, KC-enriched fraction of liver nonparenchymal cells from mice tolerized 1 month earlier by DNP-BSA pretreatment. These findings implicate KC as a primary and sustained inducer of tolerance against DNP-protein adducts and suggest a similar role in modulating allergic reactions against drug-protein adducts. Perhaps genetic and/or environmental factors affecting the activities of these cells may play a role in determining individual susceptibility to DIARs.     

Inhibitory effects of nardostachin on nitric oxide, prostaglandin E2, and tumor necrosis factor-alpha production in lipopolysaccharide activated macrophages

Nardostachin, which is an iridoid isolated from Patrinia saniculaefolia, was examined by assessing its effect on the production of tumor necrosis factor-alpha (TNF-alpha) and expression of 2 enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in lipopolysaccharide (LPS)-stimulated Raw264.7 macrophages. This compound consistently inhibited the production of nitric oxide (NO) and TNF-alpha production in a dose-dependent manner, with respective IC(50) values of 12.3 and 16.2 microM. The decrease in quantity of NO products was accompanied by a decrease in the iNOS protein level, as assessed by Western blotting probed with specific anti-iNOS antibodies. In addition, this compound also reduced the COX-2 protein expression level and the attendant PGE(2) production in LPS-stimulated macrophages. These results suggest that nardostachin may be useful for inhibiting the production of inflammatory mediators such as TNF-alpha, NO and PGE(2) in inflammatory diseases.     

Increased activity of cyclooxygenase-2 signals early neurodegenerative events in the rat retina following transient ischemia

Following transient retinal ischemia, there is neuronal cell death, breakdown of the blood-retinal barrier, activation of microglia and infiltration by hematogenous cells. The early appearance of cyclooxygenase-2 (COX-2) following an ischemic event may be responsible for signaling some of the responses that lead to neurodegeneration. We have determined the time courses of changes in protein levels and cellular localizations of COX-2 in the rat retina after transient ischemia. In the normal rat retina, COX-2 immunoreactivity was present in neurons in the INL and ganglion cell layer (GCL). Six to 12 hr after ischemia, COX-2 immunoreactivity was upregulated/induced in horizontal cells, amacrine cells, retinal ganglion cells, displaced amacrine cells of the INL and GCL, and Müller cells. The NMDA-receptor antagonist, MK801, blocked the increased COX-2 protein level and COX-2 immunoreactivity in neurons of the INL and GCL, but did not affect the induction of COX-2 in Müller cells after ischemia. The selective COX-2 inhibitor, SC-58236, prevented apoptotic cell death and was neuroprotective against loss of retinal ganglion cells after ischemia. Following transient ischemia, the selective COX-2 inhibitor did not prevent breakdown of the blood-retinal barrier or activation of microglia. However, the selective COX-2 inhibitor reduced infiltration of hematogenous cells into the retina. These results suggest that the early, increased activity of COX-2 signals neurodegenerative events following retinal ischemia.     

Effect of an acrylic posterior chamber intraocular lens on posterior capsule opacification in cataract patients with associated risk factors

PURPOSE: To evaluate the effect of an acrylic foldable posterior chamber intraocular lens (PC IOL) on the rate of posterior capsule opacification (PCO) in patients with associated risk factors. SETTING: Department of Ophthalmology, Seoul National University, Seoul, Korea. METHODS: The medical records of 570 patients who had phacoemulsification and foldable PC IOL implantation by the same surgeon from January 1, 1998, to December 31, 1999, were reviewed. Patients with risk factors for PCO (ie, young age, diabetes mellitus) received an acrylic PC IOL to decrease the opacification rate. Their rate was compared to that in patients without associated risk factors who received a foldable silicone PC IOL. RESULTS: In the patients without diabetes mellitus, the PCO rate in patients younger than 60 years with an acrylic PC IOL and in patients older than 60 years with a silicone PC IOL were similar. In patients older than 60 years, the rate of PCO was significantly lower in patients with diabetes mellitus and an acrylic PC IOL than in patients without diabetes mellitus with a silicone foldable PC IOL. CONCLUSIONS: The rate of PCO in patients with risk factors for PCO with an acrylic PC IOL was similar to or lower than that in patients without risk factors with a foldable silicone PC IOL. Therefore, acrylic PC IOLs are preferable, particularly in patients with risk factors for PCO.     

Hydrolysis of bimatoprost (Lumigan) to its free acid by ocular tissue in vitro.

We determined whether bimatoprost, which has been reported to act via putative prostamide receptors, could be hydrolyzed to its free acid (17-phenyl-PGF(2 alpha)), a potent FP receptor agonist, by human ocular tissue in vitro. We developed a gas chromatography/mass spectrometric method to measure 17-phenyl-PGF(2 alpha) levels at sub-picomolar levels. We then analyzed the amount of 17-phenyl-PGF(2 alpha) present after incubation of 50 microl Lumigan (0.03% bimatoprost) with eye tissue using this assay. We found that cornea, sclera, iris, and ciliary body, all rapidly hydrolyzed bimatoprost to 17-phenyl-PGF(2 alpha) with linear kinetics at a rate of 6.3, 2.0, 2.8, and 1.5 pmol mg tissue(-1) hr(-1), respectively. For cornea, sclera, and ciliary body, this linear rate of hydrolysis continued over a period of at least three hours, while iris-induced hydrolysis did not continue beyond one hour. Our findings suggest that bimatoprost can act as prodrug for FP receptor activation and questions the concept of a "prostamide receptor" agonist.     

Protection by the Chinese prescription Wen-Pi-Tang against renal tubular LLC-PK1 cell damage induced by 3-morpholinosydnonimine

We investigated the effects of Wen-Pi-Tang extract on the protective mechanisms of renal tubular LLC-PK1 cells, as renal tubular cells are the most vulnerable renal tissue to oxidative stress. Exposure to 800 microM 3-morpholinosydnonimine (SIN-1) resulted in a marked increase in cellular peroxynitrite (ONOO-), which converted nonfluorescent dihydrorhodamine 123 to fluorescent rhodamine 123, a detectable probe for the long-lived ONOO-. In addition, it resulted in apoptotic cell death, assessed by a DNA fragmentation assay. However, treatment with Wen-Pi-Tang extract, at concentrations of 50 and 100 microg mL(-1) together with SIN-1 protected renal tubular cells against ONOO- through scavenging ONOO- and inhibiting apoptotic cell death in a dose-dependent manner. Moreover, treatment with Wen-Pi-Tang extract both before and after exposure to SIN-1 was also protective: it reduced cellular ONOO- levels, increased cell viability and decreased the DNA fragmentation rate. These results suggest that Wen-Pi-Tang would have protective activity against ONOO- -induced renal tubular injury through the inhibition of ONOO- production and apoptotic cell death by both preventing and treating renal injury. Furthermore, morphological characteristics of apoptosis were observed in SIN-1 treated tubular cells, while the addition of Wen-Pi-Tang extract with SIN-1 attenuated these morphological changes. ONOO- generated by SIN-1 also disturbed the cell cycle by decreasing the cellular G2/M phase ratio, while Wen-Pi-Tang extract regulated the cell cycle by G2/M phase arrest.     

Cerebrosides from longan arillus

From the pulp of Euphoria longana (Longan Arillus), three cerebroside molecular species have been isolated. Six known cerebrosides, soyacerebrosides I and II, 1-O-beta-D-glucopyranosyl-(2S,3R,4E,8E)-2-(2'-lignoceroylamino)-4,8-octadecadiene-1,3-diol (longan cerebroside I) and its 8Z isomer (longan cerebroside II), momor-cerebroside I, and phytolacca cerebroside, were identified as major components of these cerebroside molecular species. All the cerebrosides were shown to be a mixture of geometrical isomers (8E and 8Z) of sphingosine-type or phytosphingosine-type glucocerebrosides possessing 2-hydroxy fatty acids. The structures of these cerebrosides have been determined on the basis of chemical and spectroscopic evidence.